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Gastric cancer (GC) is one of the most common types of malignancy worldwide, with high morbidity and mortality rates. The dysregulation of microRNAs (miRs) has been found to be involved in the carcinogenesis of GC. The present study aimed to investigate the underlying association between GC and miR-320a. Analysis using reverse transcription quantitative polymerase chain reaction indicated that the expression of miR-320a was downregulated and the expression of RAB14 was upregulated in GC tissues and cells, compared with the corresponding controls. MTT, colony formation assays, and flow cytometric analyses were used to evaluate the effect of miR-320a on cell proliferation and the cell cycle. The ectopic expression of miR-320a using miR-320a mimics suppressed cell viability, inhibited G1/S transition, and induced apoptosis in AGS and MKN45 cells. In addition, RAB14 was identified as a direct target gene of miR-320a, according to the results of bioinformatics analysis and a luciferase reporter assay. Downregulation of RAB14 by RAB14-small interfering RNA inhibited the viability of GC cells, which was similar to the phenotype of miR-320a mimics. Furthermore, the reintroduction of RAB14 partially abrogated the miR-320a-mediated downregulation of RAB14 and rescued the miR-320a-induced effects on GC cell growth. These findings suggest a potential novel therapeutic target for the treatment of GC.

miR-320a serves as a negative regulator in the progression of gastric cancer by targeting RAB14